Native Microbiota Stave Off Infection
University of British Columbia ♦ Published in PLoS ONE, October 28, 2011
Genetics can contribute to host susceptibility to microbial infection but are there other causes? A growing body of evidence points to the composition of microbial flora in the intestine as a key factor in how mammals respond to foreign pathogens. In this study out of the University of British Columbia researchers investigated the effect that infection with a common pathogen had on a number of different strains of mice with widely varying genetic backgrounds. As would be expected the mice responded differently after oral exposure. Some mice were resistant to infection while others became very sick, or even died. However, it wasn’t only genetics at work. Transplantation of microbial samples from the intestines of resistant mice into those of lethally susceptible mice prolonged microbial colonization and death, illustrating the importance that the microbial ecosystem has in regulating mucosal immunity and intestinal health.
Selection of Cardiomyocytes with SIRPA
McEwen Centre for Regenerative Medicine (UHN) ♦ University of Toronto ♦ Monash University
Published in Nature Biotechnology, October 23, 2011
Gordon Keller’s lab has discovered a protein, known as signal-regulatory protein alpha (SIRPA), that can enrich for embryonic stem cell and iPS cell-derived cardiomyocytes at purities as high as 98%. Keller, who was the first researcher to produce functional heart cells from human embryonic stem (hES) cells, has spent years investigating the developmental path that leads to the cardiac identity. In order to find this specialized protein marker researchers carried out a screen of cardiomyocytes against a panel of some 380 CD antibodies. SIRPA was found to be expressed specifically on cardiomyocytes that were the progeny of hES cells or iPS cells; the protein will allow for rapid and efficient separation of cardiomyocytes from both primitive cell types.
Engineering Therapeutic Viruses for Greater Impact
Children’s Hospital of Eastern Ontario Research Institute ♦ University of Ottawa ♦ Ottawa Hospital Research Institute ♦ OICR ♦ McGill
Published in Cancer Cell, October 18, 2011
Viruses are now being leveraged in order to target and destroy cancer cells in the body. Termed “oncolytic” viruses, these treatments not only infect and burst cancer cells but also alert the host’s immune system to the presence of the tumour ensuring a continued onslaught following administration. In hopes of improving upon oncolytic viruses currently under development, researchers have implemented functional genomics to glean information related to virus-tumour interactions. A genome-wide RNAi screen identified the endoplasmic reticulum (ER) stress response as a mechanism by which tumour cells resist the effects imposed by oncolytic viruses. Inhibiting the ER stress response pathway sensitized resistant tumour cells and increased the efficacy of oncolytic viruses by up to 10,000 fold in some cases.